Problem Description

The eye is firm to the touch as it is pumped up, like a football,
by the ciliary body that secretes a fluid (the aqueous) from behind
the iris. If the pressure rises too high then this leads to selective
death of the axons that exit the eye. These axons exit as the optic
nerve and leave the eye at a particular spot called the optic nerve
head. At this point, the firm outer layer of the eye, the sclera, is
perforated to let the axons pass through, but as a consequence of
these perforations, the sclera is weak and will accordingly deform
(the scleral sieve through which the axons pass is called the lamina
cribrosa). Not only do the axons go from an area of one pressure to
another, but they also undertake a sharp right angle change in
direction. In glaucoma, the lamina cribrosa deforms backwards.
Haemorrhages can occur at the optic nerve head and, as a consequence
of both cell death and this backward deformation, the nerve head will
appear "cupped".

This problem is to assemble a model of the back of the eye that has
four compartments: the intraocular space; the optic nerve; the
vascular space; and the outside. The Study Group is asked to look at
flow of blood and of axoplasm as they traverse these compartments and
to look for potential blocks in the flow. The aim is to see if there
are spots where either the blood vessels or the axons experience high
internal pressure that could, in turn, lead to rupture. Rupture of
capillaries would be a convincing explanation for the observed
haemorrhages at the optic nerve head and would be a novel and
plausible explanation for the observed optic nerve fibre death
observed in these conditions.

Study Group Report

We have constructed a model of how the axons of retinal ganglial
cells respond to the difference between the intraocular pressure and the
CSF pressure that is characteristic of glaucoma and papilloedema. The
model uses Poiseuille's law to describe flow along the axon, taking
into account water driven through the membrane surrounding the axon by
a difference in hydrostatic and osmotic pressures across the membrane.
In addition to our model of fluid flow in the axon, we developed a
model of the mechanical deformation of the axon in response to
hydrostatic pressure differences, and shear forces induced by flow.